Litwin S D
Cornell University Medical College, New York, New York, USA.
Scand J Immunol. 1980;11(1):15-22. doi: 10.1111/j.1365-3083.1980.tb00203.x.
Suppressor cell activity in two individuals (S1 and S2) with immunodeficiency with thymoma (ID-THY) was studied in peripheral blood mononuclear cells in pokeweed mitogen-stimulated single culture and cocultures. Secreted Ig was measured by radioincorporation and immunoprecipitation after 5-7 days. Control cocultures of normal/normal cells showed, in most cases, a percentage observed to expected ratio (% O/E) of cpm Ig near 100%. However, augmentation (% of O/E > 150) was often encountered, whereas suppression (% O/E < 50) was found only once in forty-two cocultures. In ID-THY/normal cell cocultures the degree of suppression by ID-THY cells varied widely when the same or different cocultivants were retested. This finding could be explained in part by an inverse correlation between the amount of secreted Ig produced by normal cells in single culture and the degree of suppression of the same normal by ID-THY cells in cocultures. A panel of normal cells were all suppressed when a range of S1 or S2/normal cell ratios were tested, weighing against genetic differences in suppressibility in the above system. ID-THY cells failed to block Ig secretion of human lymphoblastoid line cells, suggesting that the mechanism of suppression was related to a block in differentiation rather than interference with Ig synthesis per se. An experiment using cocultivants separated by a Millipore membrane showed that suppression was mediated by a humoral factor.
在有丝分裂原刺激的单一培养和共培养中,研究了两名患有胸腺瘤免疫缺陷(ID - THY)个体(S1和S2)外周血单核细胞中的抑制细胞活性。5 - 7天后,通过放射性掺入和免疫沉淀法测量分泌的Ig。正常/正常细胞的对照共培养在大多数情况下,cpm Ig的观察到的预期比率(% O/E)接近100%。然而,经常出现增强(% O/E > 150),而在42次共培养中仅发现一次抑制(% O/E < 50)。在ID - THY/正常细胞共培养中,当对相同或不同的共培养物进行重新测试时,ID - THY细胞的抑制程度差异很大。这一发现部分可以通过单一培养中正常细胞分泌的Ig量与共培养中ID - THY细胞对相同正常细胞的抑制程度之间的负相关来解释。当测试一系列S1或S2/正常细胞比率时,一组正常细胞均受到抑制,这排除了上述系统中抑制性的遗传差异。ID - THY细胞未能阻断人淋巴母细胞系细胞的Ig分泌,表明抑制机制与分化受阻有关,而非直接干扰Ig合成。一项使用由微孔膜分隔的共培养物的实验表明,抑制是由一种体液因子介导的。